Elevated cTnI Levels Research Articles

Platelet-to-Lymphocyte Ratio as a Potential Diagnostic Marker for Acute Coronary Syndromes in Resource-Limited Settings: A Cross-Sectional Study from Single Center in Banten, Indonesia

Background: Acute coronary syndrome (ACS) poses a significant global health burden, particularly in resource-limited settings where access to advanced diagnostic tools is often constrained. The platelet-to-lymphocyte ratio (PLR), a simple and readily available marker from routine blood tests, has shown promise as a potential diagnostic tool for ACS. This study aimed to evaluate the diagnostic accuracy of PLR in identifying ACS patients in a resource-limited setting in Indonesia. Methods: A cross-sectional study was conducted at Hermina Periuk Hospital, Tangerang, Banten, Indonesia, between December 2020 and December 2022. Patients presenting to the Emergency Room with a diagnosis of ACS were included. PLR was calculated from complete blood count data, and cardiac troponin I (cTnI) served as the gold standard for ACS diagnosis. The diagnostic performance of PLR in predicting elevated cTnI levels was assessed. Results: Of the 121 patients initially identified, 39 met the inclusion and exclusion criteria. Elevated PLR values (>116) were observed in 25 patients (64.1%), while 15 patients (38.5%) had elevated cTnI levels. A statistically significant correlation was found between elevated PLR and elevated cTnI (p = 0.018). No significant association was observed between neutrophil-to-lymphocyte ratio (NLR) and elevated cTnI. Conclusion: PLR demonstrates potential as a diagnostic marker for ACS in resource-limited settings. Its simplicity, accessibility, and cost-effectiveness make it a valuable tool for early identification and risk stratification of ACS patients, particularly in areas with limited access to advanced cardiac diagnostics.

A-017 Clinical Performance Evaluation of the Atellica IM High-Sensitivity Troponin I Assay to Aid in Risk Stratification for All-Cause Mortality and Major Adverse Cardiac Events

Abstract Background Cardiac troponin I (cTnI) is the only troponin isoform present in the myocardium, where it binds to actin and inhibits actin and myosin interaction. Upon myocardial injury, cTnI is released into circulation and serial measurements can be used to aid in the diagnosis of acute myocardial infarction (AMI). In addition, in patients presenting with signs and symptoms of acute coronary syndrome (ACS), elevated cTnI levels provide useful prognostic information relative to short and long-term risk of all-cause mortality (ACM) and major adverse cardiac events (MACE). The objective of this study was to evaluate the clinical performance of the Atellica® IM TNIH assay to aid in risk stratification for ACM/MACE*. Methods Patients from 29 emergency departments (ED) across the United States presenting with signs and symptoms suggestive of ACS were followed for 30-, 90-, and 365-day progression to ACM/MACE (consisting of myocardial infarction, urgent revascularization, cardiac death, or heart failure hospitalization). At each timepoint, the risk (cumulative incidence) and hazard ratios were calculated for populations with baseline cTnI levels ≤ or > the 99th percentile value. Kaplan-Meier curves were generated to display the absolute risk (cumulative incidence) of ACM/MACE outcomes. Analyses were performed for all enrolled patients (entire population) and separately for the entire population excluding those with an adjudicated AMI at presentation. Analyses were performed separately for both serum and plasma (lithium heparin) sample types. Results For the Entire Population cohort, the binary baseline TNIH result (TNIH > overall 99th percentile or ≤ overall 99th percentile) was significantly associated with 30-, 90-, and 365-day cumulative ACM/MACE (p-value<0.0125) for both plasma and serum samples. For plasma samples, risk difference increased from 6.27% at day 30 to 19.62% at day 365. For serum samples, risk difference increased from 6.24% at day 30 to 18.71% at day 365. Cox proportional hazard regression analysis compared the TNIH 99th percentile groups in their hazard of experiencing an ACM/MACE event in the 30-, 90-, and 365-days post ED presentation. For plasma samples, the hazard of ACM/MACE for subjects with cTnI values above the TNIH 99th percentile was relatively constant at each follow-up interval as more than double the rate of subjects below the 99th percentile; hazard ratios ranged between 2.81 (p-value<0.0001) and 3.49-fold (p-value<0.0001) for the three follow up visits. For serum samples, the hazard ratios were between 2.69 (p-value<0.0001) and 3.28-fold (p-value<0.0001) for the three follow up visits. Similar results were obtained for the Entire Population Excluding Subjects with Adjudicated AMI During Initial Presentation cohort. Conclusions The Atellica IM TNIH assay can be used in the detection of myocardial injury and can aid in risk stratification for 30-, 90-, and 365-day all-cause mortality (ACM) and major adverse cardiac events (MACE) in patients presenting with signs and symptoms suggestive of acute coronary syndrome (ACS). *This prognostic claim is not available in the United States.

Correlation between serum cardiac troponin I level and PDAI score in patients with pemphigus vulgaris.

Pemphigus vulgaris (PV) is a rare, yet serious autoimmune disorder primarily affecting the skin and mucous membranes. While the dermatological and mucosal aspects of PV are well-documented, the potential for systemic involvement, particularly cardiac complications, remains under-explored. This study aimed to investigate the serum cardiac troponin I (cTnI) level in patients with PV versus healthy controls. The relationship between serum cardiac troponin I (cTnI) levels and various demograpgics, clinical and laboratory characteristics in patients with PV was also dealt with. This cross-sectional study was conducted on 59 patients with pemphigus vulgaris and 59 age- and sex- matched healthy controls, visited at a tertiary care hospital from August 2021 to May 2023. After thorough history taking and physical examination, troponin level was measured by the ECL (Electrochemiluminescence) method. The correlation between serum cTnI level and various variables was evaluated using Pearson's correlation coefficient. The mean serum cardiac troponin I (cTnI) level in patient group was 0.104 ± 0.05 ng/mL, with a range of 0.01 to 0.25 ng/mL. Despite mean cTnI level in patients was greater than controls, this difference was not reach to the significance level (P value: 0.058). The analysis revealed a significant positive correlation (r = 0.52, p = 0.005310), suggesting that higher PDAI scores were associated with elevated cTnI level. The correlation between serum cardiac troponin I (cTnI) level and PDAI score, even without any clinical sign or risk factor for cardiovascular disease suggests a potential link between the severity of PV and subtle cardiac involvement, highlighting the importance of cardiac monitoring in these patients.

Elevated Cardiac Troponin I Level Associated to Cardiac Dysfunction in Burned Patients.

Severely burned patients often develop cardiac dysfunction and heart failure. The purpose of this retrospective study is to evaluate the role of cardiac troponin I (cTI) and its association to patients with burns. Patients deidentified data were collected from a national database in May 2023. Adult patients with burns who had cTnI lab counted were enrolled in this study. Patients were grouped by the cTnI mean level within 72 h including patients with elevated cTnI levels at >0.3 ng/mL (n = 2188 patients) and patients with nonelevated cTnI level (<0.04 ng/mL) (n = 3200). The cohorts were further stratified by less than 20% TBSA mild burn population and >20% TBSA severe burn population to replicate the severity of burns. The 30-day incidences of acute myocardial infarction (MI), sepsis, and mortality were investigated after the cohorts were propensity-matching balanced. The odds ratios (ORs) with 95% CI for MI were (9.829/7.081-13.645), sepsis (1.527/1.269-1.959), and mortality (2.586/2.110-3.170), respectively (P < .05). The groups that were further stratified into mild burn and severe burn had the following results: The mild burn ORs and 95% CI for MI was (6.237/3.986-9.785), sepsis (1.603/1.132-2.270), and mortality was (2.298/1.629-3.242). The severe burn cohort had ORs and 95% CI for MI (3.145/1.469-6.732), sepsis (0.993/0.555-1.777), and mortality (2.934/1.924-4.475). In conclusion, the patients with earlier elevated cTnI levels had worse outcomes of MI and mortality in both severe and mild burns.

Relationship Between Heart Rate Variability Parameters and Short-Term Prognosis of Patients with Acute Myocardial Infarction.

To determine the link between heart rate variability (HRV) and short-term adverse outcomes (re-hospitalisation or death due to cardiac arrhythmia, recurrent myocardial infarction, heart failure, all-cause death) in acute myocardial infarction (AMI). A descriptive study. Place and Duration of the Study: Department of Cardiovascular Medicine, The First Affiliated Hospital of Anhui Medical University, China, from January 2018 to December 2021. Clinical data of 245 patients diagnosed with AMI were retrospectively analysed. After discharge from the hospital, patients were followed for a year and categorised into two groups based on the occurrence of adverse events: the adverse event group (n=82) and the no adverse event group (n=163). Differences in clinical characteristics were compared, independent factors influencing adverse events were analysed, and diagnostic efficacy was assessed. Univariate analysis showed age, hyperlipidaemia, specific HRV parameters (SDNN, SDANN, RMSSD, PNN50, LF/HF), and myocardial injury markers (CK-MB, cTnI, NT-proBNP) as associated with these events (all p < 0.05). Multivariable analysis revealed decreased SDNN, decreased SDANN, increased LF/HF, and elevated levels of CK-MB, cTnI, and NT-proBNP as independent influences. Both HRV parameters and myocardial injury markers were reliable predictors on ROC curve analysis. The highest diagnostic efficacy was achieved by combining these predictors. AMI patients frequently experience short-term adverse events. Both HRV parameters and myocardial injury markers, which demonstrate significant predictive efficacy, independently influence these outcomes. Acute myocardial infarction, Coronary angiography, Heart rate variability, Myocardial injury, Risk factors.

Types of Septic Cardiomyopathy: Prognosis and Influencing Factors - A Clinical Study.

To explore the prognostic outcomes associated with different types of septic cardiomyopathy and analyze the factors that exert an influence on these outcomes. The data collected within 24 hours of ICU admission included cardiac troponin I (cTnI), N-terminal pro-Brain Natriuretic Peptide (NT-proBNP); SOFA (sequential organ failure assessment) scores, and the proportion of vasopressor use. Based on echocardiographic outcomes, septic cardiomyopathy was categorized into left ventricular (LV) systolic dysfunction, LV diastolic dysfunction, and right ventricular (RV) systolic dysfunction. Differences between the mortality and survival groups, as well as between each cardiomyopathy subgroup and the non-cardiomyopathy group were compared, to explore the influencing factors of cardiomyopathy. A cohort of 184 patients were included in this study, with LV diastolic dysfunction having the highest incidence rate (43.5%). The mortality group had significantly higher SOFA scores, vasopressor use, and cTnI levels compared to the survival group; the survival group had better LV diastolic function than the mortality group (p < 0.05 for all). In contrast to the non-cardiomyopathy group, each subgroup within the cardiomyopathy category exhibited elevated levels of cTnI. The subgroup with left ventricular diastolic dysfunction demonstrated a higher prevalence of advanced age, hypertension, diabetes mellitus, coronary artery disease, and an increased mortality rate; the RV systolic dysfunction subgroup had higher SOFA scores and NT-proBNP levels, and a higher mortality rate (P < 0.05 for all); the LV systolic dysfunction subgroup had a similar mortality rate (P > 0.05). Patients with advanced age, hypertension, diabetes mellitus, or coronary artery disease are more prone to develop LV diastolic dysfunction type of cardiomyopathy; cardiomyopathy subgroups had higher levels of cTnI. The RV systolic dysfunction cardiomyopathy subgroup had higher SOFA scores and NT-proBNP levels. The occurrence of RV systolic dysfunction in patients with sepsis significantly increased the mortality rate.

Cardiac troponin I as predictor for cardiac and other mortality in the German randomized lung cancer screening trial (LUSI)

Cardiac Troponin I (cTnI) could be used to identify individuals at elevated risk of cardiac death in lung cancer (LC) screening settings. In a population-based, randomized LC screening trial in Germany (“LUSI” study) serum cTnI was measured by high-sensitivity assay in blood samples collected at baseline, and categorized into unquantifiable/low (< 6 ng/L), intermediate (≥ 6–15 ng/L), and elevated (≥ 16 ng/L). Cox proportional-hazard models were used to estimate risk of all-cause and cardiac mortality with cTnI levels. After exclusion criteria, 3653 participants were included for our analyses, of which 82.4% had low, 12.8% intermediate and 4.8% elevated cTnI, respectively. Over a median follow up of 11.87 years a total of 439 deaths occurred, including 67 caused by cardiac events. Within the first 5 years after cTnI measurement, intermediate or elevated cTnI levels showed approximately 1.7 (HR = 1.69 [95% CI 0.57–5.02) and 4.7-fold (HR = 4.66 [1.73–12.50]) increases in risk of cardiac death relative to individuals with unquantifiable/low cTnI, independently of age, sex, smoking and other risk factors. Within this time interval, a risk model based on age, sex, BMI, smoking history and cTnI showed a combined area under the ROC curve (AUC) of 73.6 (58.1–87.3), as compared to 70.4 (53.3–83.5) for a model without cTnI. Over the time interval of > 5–10 years after blood donation, the relative risk associations with cTnI and were weaker. cTnI showed no association with mortality from any other (non-cardiac) cause. Our findings show that cTnI may be of use for identifying individuals at elevated risk specifically of short-term cardiac mortality in the context of LC screening.

Role of Biomarkers of Myocardial Injury to Predict Adverse Outcomes in Hypertrophic Cardiomyopathy.

Serum troponins and CK-MB (creatine kinase-MB) are readily detectable and reliable cardiac-specific biomarkers of subclinical myocardial injury. This study explores the roles of cTnI (cardiac troponin I) and CK-MB in hypertrophic cardiomyopathy (HCM). This study included 1045 patients with HCM who had baseline cTnI and CK-MB measurements at Fuwai Hospital between 1999 and 2019. Patients were excluded if they had undergone percutaneous coronary intervention or coronary artery bypass grafting, or had renal failure. Five end points were studied: all-cause death, cardiovascular death, noncardiovascular death, sudden cardiac death, and other cardiovascular death. Cox regression was used to assess the associations of cTnI and CK-MB levels with outcomes. Nine hundred seventy patients with available follow-up data were finally analyzed (mean age, 49.3 years; 36.4% female). During the median 4.3-year follow-up period, 87 patients reached the end points. Higher cTnI (per 0.05 ng/mL increase) and CK-MB (per 1 IU/L increase) levels were associated with increased risks of all-cause death (cTnI: adjusted hazard ratio [HR], 1.038, P<0.001; CK-MB: adjusted HR, 1.021, P=0.004), cardiovascular death (cTnI: adjusted HR, 1.040, P<0.001; CK-MB: adjusted HR, 1.025, P=0.006), and sudden cardiac death (cTnI: adjusted HR, 1.045, P<0.001; CK-MB: adjusted HR, 1.032, P=0.001). Patients with elevated levels of both cTnI and CK-MB had worse prognoses than patients with an elevated level of either biomarker alone and patients who did not have an elevated level of either biomarker. Addition of the binary indicator elevation of both cTnI and CK-MB significantly improved the discrimination and reclassification abilities of the standard HCM Risk- sudden cardiac death model (C statistics: P=0.002; net reclassification improvement, 0.652; integrated discrimination improvement, 0.064). Comprehensive evaluations of biomarkers of myocardial injury, cTnI and CK-MB, have considerable value for predicting adverse outcomes among patients with HCM. Routine cTnI and CK-MB assessments may help to guide implantable cardioverter defibrillator implantation for primary prevention in HCM.

Increased cTnI Predicts Early Death in Patients with Severe Fever with Thrombocytopenia: A Multicenter Study in North China.

Myocardial injury is common in severe fever with thrombocytopenia syndrome (SFTS) patients. Currently, research on the prognostic value of cardiac troponin I (cTnI) for predicting the mortality of SFTS patients, especially death within 7 days is limited. Between May 2011 and October 2022, clinical and laboratory data on admission of consecutive SFTS cases were collected from six medical centres in China. The clinical endpoint was in-hospital all-cause death within seven days. Risk factors of myocardial injury and death were analysed using multivariable regression models. Prognostic models were established using Cox regression and performance of indicators was evaluated in terms of calibration, discrimination. A total of 1379 laboratory-confirmed patients were enrolled, in which 686 subjects were included for analysis. The median age was 66 years, with 48.1% of male. Eighty-seven patients died within seven days and 396 patients diagnosed with myocardial injury during hospitalization. Non-survivors had significant higher levels of cardiac indices than survivors, including cTnI, aspartic transaminase (AST) and lactate dehydrogenase (LDH). Elevated levels of cTnI (HR = 1.058, 95% CI:1.032-1.085), AST (HR = 1.191, 95% CI:1.150-1.234) and LDH (HR = 1.019, 95% CI:1.009-1.029) predicted risk of early in-hospital mortality. cTnI model performed best, with area under curve of 0.850 (0.774-0.926) and concordance index of 0.842, respectively. Statistical differences were found between high and low levels of cTnI for mortality (P<0.001) using 0.35 ng/mL as the optimal cut-off. The risk of early in-hospital death can be predicted by cTnI. Clinical doctors should remind vigilant concerning the elevation of cardiac enzyme as soon as possible.

IL-6 and D-dimer Levels at Admission Predict Cardiac Injury and Early Mortality during SARS-CoV-2 Infection

Background: We previously described the mortality associated with cardiac injury in patients with coronavirus disease 2019 (COVID-19). The activation of immune and thrombotic biomarkers at admission, and their ability to predict cardiac injury and mortality patterns in COVID-19, remains unclear. Methods: This retrospective cohort study included 170 patients with COVID-19 with cardiac injury at the time of admission to Tongji Hospital in Wuhan between January 29, 2020, and March 8, 2020. The temporal evolution of inflammatory cytokines, coagulation markers, clinical treatment, and mortality were analyzed. Continuous variables are expressed as median (interquartile range). The Mann-Whitney test was used for two-group comparisons, whereas the Kruskal-Wallis test was used for comparisons among three groups. Categorical variables are expressed as proportions and percentages, and Fisher’s exact test was used to compare differences. A multivariate regression model was used to predict in-hospital death. A simple linear regression analysis was applied to examine the correlation between baseline biomarkers and peak cTnI levels. Results: Of the 170 patients, 60 (35.3%) died early (&lt;21 d), and 61 (35.9%) died after a prolonged stay. The admission laboratory findings correlating with early death were elevated interleukin 6 (IL-6) (P &lt; 0.0001), tumor necrosis factor-α (P = 0.0025), and C-reactive protein (P &lt; 0.0001). We observed the trajectory of biomarker changes in patients after admission hospitalization, and determined that early mortality was associated with a rapidly increasing D-dimer level, and gradually decreasing platelet and lymphocyte counts. Multivariate and simple linear regression models indicated that the risk of death was associated with immune and thrombotic pathway activation. Elevated admission cTnI levels were associated with elevated IL-6 (P = 0.03) and D-dimer (P = 0.0021) levels. Conclusion: In patients with COVID-19 with cardiac injury, IL-6 and D-dimer levels at admission predicted subsequently elevated cTnI levels and early death, thus highlighting the need for early inflammatory cytokine-based risk stratification in patients with cardiac injury.

Exercise-induced troponin I elevation is associated with alterations in regional longitudinal strain

Abstract Background Mechanisms of exercise-induced troponin elevation in healthy individuals are unclear. This study aimed to determine if exercise-induced cardiac troponin elevation (cTn) is associated with alterations in the myocardial response to physical stress. Methods This study assessed regional and global myocardial function by strain echocardiography at rest and following exercise of increasing workloads in individuals with either a high- or a normal cTnI response to exercise. High-cTnI responders (n=34) were individuals with a previous exercise-induced cTnI level above the 92.5% limit (cTnI &amp;gt; 200 ng/L) in the NEEDED population (n= 1002). Normal-cTnI responders comprised 25 reference individuals with a post-exercise cTnI &amp;lt; 200 ng/L. All study participants were healthy individuals with normal CT coronary angiography. The first exercise was a cardiopulmonary exercise test (CPET) of 43 (40,45) minutes. The second exercise was a 91 km recreational mountain bike race of 230 (210, 245) minutes. Myocardial function was assessed by echocardiography before and within 10 minutes and 24 hours after both exercises. Results Study individuals were 51±10 years old, and 46 (74 %) were male. At baseline, there were no differences between the High- and Normal-cTnI responders regarding demographics, training condition, cardiac risk factors, peak oxygen consumption and conventional echocardiographic parameters. Maximal cTnI levels 3 hours after exercise were significantly higher in the High- compared with Normal-cTnI responders: CPET: cTnI 13 (9-32) vs 9 (5-17) ng/L (p 0.027) and Race: cTnI: 101 (76-198) vs 37 (25-69) ng/L (p &amp;lt;0.001). Following exercise, there were no differences in global ventricular function between the two groups, assessed as left ventricular (LV) global longitudinal strain (GLS) and right ventricular (RV) GLS. When comparing regional longitudinal strain between the two groups, High-cTnI responders had significantly lower regional strain values in the anteroseptal segments following both exercises (p-values 0.005-0.041, 8-14% relative difference, Figure 1 and 2). The changes were more profound after the most intensive exercise (the Race). Conclusion High-cTnI responders have larger reductions in post-exercise systolic longitudinal strain in anteroseptal segments than Normal -cTnI responders. The reduction in regional strain was most profound following the highest workload (the Race). These findings suggest that highly elevated exercise-induced cTnI levels may reflect vulnerable regional alterations in the myocardial response to increasing workloads.Figure 1CPETFigure 2Race

Effect of Sulforaphane on cardiac injury induced by sepsis in a mouse model: Role of toll-like receptor 4.

As sepsis is associated with a 50% increase in mortality, sepsis-induced cardiomyopathy has become a critical topic. A multidisciplinary approach is required for the diagnosis and treatment of septic cardiomyopathy. This study looked at Sulforaphane, a natural product that aims to evaluate cardiac function after sepsis, and its likely mechanism of action. Twenty-four adult male Swiss albino mice were randomly divided into 4 equal groups (n=6): sham, CLP, vehicle Sulforaphane (the same amount of DMSO injected IP one hour before the CLP), and Sulforaphane group (one hour before the CLP, a 5mg/kg dose of Sulforaphane was injected). Cardiac tissue levels of toll-like receptor 4 (TLR-4), pro-inflammatory mediators, anti-inflammatory markers, oxidative stress markers, apoptosis markers, and serum cardiac damage biomarkers were assessed using ELISA. Statistical analyses, including t-tests and ANOVA tests, were performed with a significance level of 0.05 for normally distributed data. Compared to the sham group, the sepsis group had significantly elevated levels of TLR-4, IL-6, TNF-α, MIF, F2-isoprostane, caspase-3, cTn-I, and CK-MB (p<0.05). In contrast, the Sulforaphane pre-treated group demonstrated significantly lower levels of these markers (p<0.05). Additionally, Bcl-2 levels were significantly reduced (p<0.05) in the Sulforaphane group. Sulforaphane administration also significantly attenuated cardiac tissue injury (p<0.05). The findings suggest that Sulforaphane can decrease heart damage in male mice during CLP-induced polymicrobial sepsis by suppressing TLR-4/NF-kB downstream signal transduction pathways.

Prevalence of stable coronary artery disease and its associated clinical factors among patients with chest pain and elevated cardiac troponin alone

Cardiac troponin is a useful test for diagnosing cardiogenic causes in patients with chest pain. However, cardiac troponin levels are often elevated in patients with chest pain due to non-cardiac causes other than coronary artery disease. The purpose of this study was to investigate the prevalence of coronary artery disease (CAD) and its associated factors in patients with chest pain and elevated cardiac troponin I (cTnI). 104 patients (mean age, 65 ± 11 years; 60 [58%] men) who underwent coronary angiography (CAG) for chest pain and elevated cTnI levels were enrolled in this study. All patients had a normal CK-MB range and did not show any ischemic changes on electrocardiography or echocardiography. Patients were classified into two groups according to the presence of CAD (Group 1, n = 62) and the absence of CAD (Group 2, n = 42). Patients were classified into subgroups according to the presence (Group 2a, microvascular angina [MVA], n = 18) and absence (Group 2b, non-angina [NA], n = 25) of angina. CAD was diagnosed in 62 (60%) patients and MVA was suspected in 18 (17%) patients without CAD. Patients with CAD showed elevated blood pressure and slightly decreased heart rate. Diabetes mellitus was more prevalent in patients with CAD and patients without CAD (esp. with MVA) were more likely to be common drinkers. Increased relative wall thickness (RWT) and reduced E’ velocity were associated with CAD. High-density lipoprotein (HDL) levels were reduced in patients with CAD and MVA but were higher in patients with NA. Lower HDL level was found to be independently associated with the presence of CAD. Elevated cTn1 levels without other evidence of myocardial ischemia are sufficient for performing CAG in patients with stable chest pain.

Aconitum carmichaelii Debx. Attenuates Heart Failure through Inhibiting Inflammation and Abnormal Vascular Remodeling

Heart failure (HF) is the most common complication following myocardial infarction, closely associated with ventricular remodeling. Aconitum carmichaelii Debx., a traditional Chinese herb, possesses therapeutic effects on HF and related cardiac diseases. However, its effects and mechanisms on HF-associated cardiac diseases are still unclear. In the present study, a water extraction of toasted Aconitum carmichaelii Debx. (WETA) was verified using UPLC-Q/TOF-MS. The heart function of HF rats was assessed by echocardiography and strain analysis, and myocardial injury was measured by serum levels of CK-MB, cTnT, and cTnI. The pathological changes of cardiac tissues were evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin and eosin (H&E) staining, and Masson's trichrome staining. Additionally, the levels of inflammation-related genes and proteins and components related to vascular remodeling were detected by RT-qPCR, Western blot, and immunofluorescence. WETA significantly inhibited the changes in echocardiographic parameters and the increase in heart weight, cardiac infarction size, the myonecrosis, edema, and infiltration of inflammatory cells, collagen deposition in heart tissues, and also mitigated the elevated serum levels of CK-MB, cTnT, and cTnI in ISO-induced rats. Additionally, WETA suppressed the expressions of inflammatory genes, including IL-1β, IL-6, and TNF-α and vascular injury-related genes, such as VCAM1, ICAM1, ANP, BNP, and MHC in heart tissues of ISO-induced HF rats, which were further confirmed by Western blotting and immunofluorescence. In summary, the myocardial protective effect of WETA was conferred through inhibiting inflammatory responses and abnormal vascular remodeling in ISO-treated rats.

ASSESSMENT OF CARDIOPROTECTIVE EFFECT OF NECROSTATIN-1 STABLE IN A MICE MODEL OF ACUTE DOXORUBICIN-INDUCED CARDIOTOXICITY.

The aim: To evaluate the effect of Necrostatin-1s (Nec-1s), an inhibitor of necroptosis, on acute Dox-induced cardiotoxicity in a mice model. Materials and methods: Fifteen male mice were used. The animals were allocated into three groups. On the third day of the experiment, a single intraper¬itoneal dose of 20 mg/kg Dox was used to induce cardiotoxicity. Mice in the control group were given vehicle (DMSO) intraperitoneally, whereas mice in the third group were given 5 mg/kg Nec-1s two days before Dox treatment and continued for a total of five days. Animals were euthanized at the conclusion of the research. ELISA was used to assess the following parameters: cTnI, TNF-α, IL-1β, GPX-4, and Hmox-1. The expression of TNF-R1 and phosphorylated NF-κβ p65 was measured using immunohistochemistry. In addition, a histopathologic evaluation of the cardiac lesions was conducted. Results: Our results showed that Dox treatment substantially elevated serum cTnI levels, increased tissue inflammatory biomarkers (TNF-α, IL-1β, phospho NF-κβ p65 and TNF-R1), and reduced tissue antioxidant enzymes (GPX-4, Hmox-1). A histopathological analysis showed pronounced necrosis and vacuolization. These results were drastically changed by pretreatment with Nec-1s, with serum cTnI levels in this group being much lower than in the Dox group. In addition to a significant decrease in inflammatory markers, antioxidant enzymes were partially recovered. Moreover, there was preservation of the cardiac morphology to a level that was roughly normal. Conclusions: Our findings demonstrate that pretreatment with Nec-1s protected against acute Dox-induced cardiotoxicity. This cardioprotective effect was mainly due to amelioration of inflammation that reflected by inhibition of NF-κβ/TNF-α/TNF-R1 pathway, with partial restoration of antioxidant enzymes, GPX-4 and Hmox1.

Cardiac Troponin I Levels in Acute Exacerbation of COPD Patients: A Cross-sectional Study

Introduction: Chronic Obstructive Pulmonary Disease (COPD) is associated with right ventricular overloading and pulmonary hypertension. In COPD patients co-morbidities determine the outcome and quality of life. Cardiac Troponins (cTn) are suspected to be elevated in right ventricular failure. Aim: To find the incidence of cardiac Troponin-I levels and association of elevated cTnI levels with clinical outcome in acute exacerbation of COPD. Materials and Methods: The cross-sectional study comprised of 102 patients with acute exacerbation of COPD. These patients were admitted in medical wards and Intensive Care Unit (ICU) in the Department of General Medicine, Karnataka Institute of Medical Sciences Hospital, Hubli, Karnataka, India, from 2018-2020. Investigations included complete blood count, renal function tests, serum electrolytes, liver function tests, Electrocardiography (ECG), ECHO and chest X-ray. Association of cardiac troponin I and acute exacerbation of COPD was evaluated. The cTnI level ≥0.01ng/mL was considered positive. Results: The serum cTnI was found to be positive in 43 (42.2%) patients with acute exacerbation of COPD. The patients with cTnI levels ≥0.01 ng/mL had significantly higher need for Non Invasive Ventilation (NIV) 32 (74.4%), invasive ventilation support 5 (11.6%), prolonged duration of hospital stay 33 (76.7%), and higher mortality 15 (34.9%) rate as compared to patients having cTnI &lt;0.01 ng/mL. Conclusion: The cTnI is elevated in a significant subset of patients with acute exacerbation of COPD. cTnI elevation was associated with higher need for NIV and invasive ventilator support. Levels of cTnI ≥0.01 ng/mL may be considered as a biomarker to predict morbidity and mortality in acute exacerbation of COPD patients.

Serum biomarkers, including nitric oxide metabolites (NOx), for prognosis of cardiovascular death and acute myocardial infarction in an ESSE-RF case–control cohort with 6.5-year follow up

The present case–control study aimed to assess associations of routine and experimental biomarkers with risk for cardiovascular death and acute myocardial infarction (AMI) in a cohort recruited from the multicenter study “Cardiovascular Epidemiology in Russian Federation” (ESSE-RF) to identify experimental biomarkers potentially suitable for expanded evaluation. A total of 222 subjects included cardiovascular death (N = 48) and AMI cases (N = 63) during 6.5-year follow up and matched healthy controls. Seven routine and eight experimental biomarkers were assayed to analyze associations with outcomes using logistic and Cox proportional hazard regressions. Elevated levels of cardiac troponin I (cTnI), C-reactive protein (CRP), and nitric oxide metabolites (NOx) were independently associated (P < 0.001) with higher risk of cardiovascular death (estimated hazard ratio (eHR) = 1.83–3.74). Elevated levels of NOx and cTnI were independently (P < 0.001) associated with higher risk of nonfatal AMI (eHRs = 1.78–2.67). Elevated levels of angiopoietin-like protein 3 (ANGPTL3) were independently associated (P < 0.001) with lower risk of cardiovascular death (eHRs 0.09–0.16) and higher risk of nonfatal AMI (eHR = 2.07; P = 0.01). These results indicated that subsequent expanded validation should focus on predictive impact of cTnI, NOx, CRP, and ANGPTL3 to develop nationwide recommendations for individual stratification of patients with cardiovascular risks.

Preoperative cardiac troponin I as a predictor of postoperative cardiac events in patients with end stage renal disease undergoing non-cardiac surgery

We investigated if elevated cardiac troponin I (cTnI) serum levels before non-cardiac surgery were predictors of postoperative cardiac events in patients with end stage renal disease (ESRD) undergoing dialysis. In total, 703 consecutive patients with ESRD undergoing dialysis who underwent non-cardiac surgery were enrolled. Preoperative cTnI serum levels were measured at least once in all patients. The primary endpoint was defined as a composite of cardiac death, myocardial infarction (MI), and pulmonary edema during hospitalization or within 30 days after surgery in patients with a hospitalization longer than 30 days after surgery. Postoperative cardiac events occurred in 48 (6.8%) out of 703 patients (cardiac death 1, MI 18, and pulmonary edema 33). Diabetes mellitus (DM), previous ischemic heart disease, and congestive heart failure were more common in patients with postoperative cardiac events. Peak cTnI serum levels were higher in patients with postoperative cardiac event (180 ± 420 ng/L vs. 80 ± 190 ng/L, p = 0.008), and also elevated peak cTnI levels > 45 ng/L were more common in patients with postoperative cardiac events (66.8% vs. 30.5%, p < 0.001). Multivariate logistic regression analysis showed that DM (odds ratio [OR] 2.509, 95% confidence interval [CI] 1.178–5.345, p = 0.017) and serum peak cTnI levels ≥ 45 ng/L (OR 3.167, 95% CI 1.557–6.444, p = 0.001) were independent predictors for the primary outcome of cardiac death/MI/pulmonary edema. Moreover, cTnI levels ≥ 45 ng/L had an incremental prognostic value to the revised cardiac risk index (RCRI) (Chi-square = 23, p < 0.001), and to the combined RCRI and left ventricular ejection fraction (Chi-square = 12, p = 0.001). Elevated preoperative cTnI levels are predictors of postoperative cardiac events including cardiac death, MI, and pulmonary edema in patients with ESRD undergoing non-cardiac surgery.

Prognostic value of cardiac troponin in dialysis patients with paroxysmal supraventricular tachycardia.

A rise in cardiac troponin I (cTnI) is common in supraventricular tachycardia (SVT). While troponin elevation in SVT is thought to be a predictor of future adverse events in patients with prior coronary artery disease, the prognostic significance of cTnI in end-stage kidney disease (ESKD) patients with SVT are not known. We aimed to examine the prognostic significance of cTnI in ESKD patients presenting with SVT in the emergency department. This was a retrospective, multiple-center observational study utilizing regularly collected electronic medical records. We screened electronic medical records of all dialysis patients presenting to the emergency departments in 5 hospitals over 12 years with SVT. These patients were divided into whether cTnI was tested, and were further stratified into the cTnI-positive and cTnI-negative groups. The primary outcome of the study was the 3-year risk of major adverse cardiovascular events (MACE). Sixty-two patients were qualified for inclusion. Fifty-seven patients (91.9%) were tested for cTnI, and 5 patients were not. Patients with the cTnI test were older (P = .03) and had a longer length of hospital stay (P < .001). Forty-seven patients (82.5%) had a positive result, and 10 (17.5%) had a negative result. A history of hypertension (P = .013) and decreased left ventricular ejection fraction (P = .048) were the independent predictors of cTnI elevation. After a mean follow-up period of 20.6 ± 14.7 months, there were no differences in 3-year MACE between patients with or without elevated cTnI levels in Kaplan-Meier analysis (P = .34). A history of coronary artery disease was the only independent predictor of 3-year MACE (P = .017). Through the subgroup analysis, a history of coronary artery disease (HR 2.73; CI 1.01-7.41; P = .049) remained an independent risk factor for 3-year MACE in patients with elevated cTnI levels. A large proportion (82.5%) of troponin elevation was observed in ESKD patients with SVT, but it had a poor correlation with MACE.

Evaluation Value and Clinical Significance of Cardiac Troponin Level and Pediatric Sequential Organ Failure Score in the Definition of Sepsis 3.0 in Critically Ill Children.

Objective A case-control study was conducted to explore the value and clinical significance of troponin level and pediatric sequential organ failure score in the evaluation of sepsis 3.0 definition in critically ill children. Methods 180 children with sepsis who were admitted to the ICU from March 2019 to June 2021 were enrolled in our hospital as the research objects. In addition, 100 children with general infection did not meet the diagnostic criteria of systemic inflammatory response syndrome (SIRS) as controls. The creatine kinase MB (CK-MB) and cardiac troponin I (cTnI) data at the 1st and 24-72 h after admission to pediatric intensive care unit (PICU) were enrolled as the observation indexes of myocardial enzymology. In the meantime, the relevant literature was reviewed to obtain the indicators related to sepsis death. The data of the first examination in the medical history data were enrolled for analysis. According to the definition of sepsis 3.0 in critically ill children, they were assigned into sepsis and nonsepsis group. According to the survival outcome of discharge and 30 days after discharge, the patients were assigned into the death subgroup and survival subgroup and were assigned into the sequential organ failure assessment (SOFA) score ≥ 2 subgroup and< 2 subgroup according to SOFA score. COX proportional hazard regression was used to analyze the relationship between CK-MB, cTnI, and SOFA scores and prognosis. ROC curve was adopted to analyze the value of CK-MB, cTnI, and SOFA scores in the evaluation of critical sepsis in children. Results Univariate analysis indicated that the prognosis of children with sepsis was correlated with abnormal levels of CK-MB and cTnI, SOFA score, oxygenation index < 200, mean arterial pressure, and Glasgow coma scale (GCS), and the difference was statistically significant (P < 0.05). The results of COX regression analysis indicated that the variables that were remarkably associated with death from sepsis in children were CK-MB, elevated cTnI levels, and SOFA score ≥ 2, and serum cTnI and/or CK-MB levels and SOFA score were remarkably higher correlation (r = 0.453, P < 0.05). In terms of the myocardial enzyme levels in the sepsis group and the nonsepsis group, the levels of CK-MB and (or) cTnI augmented in 121/180 cases (67.22%) in the sepsis group and in 19/100 cases (19.00%) in the nonsepsis group. The levels of CK-MB and (or) cTnI were augmented, and the difference was statistically significant (P < 0.05). The levels of CK-MB and cTnI in the sepsis group at admission to ICU and 24 to 72 hours after admission were remarkably higher compared to the nonsepsis group. The levels of CK-MB and cTnI at 24-72 h were higher compared to ICU. The myocardial enzyme levels of different SOFA scores and survival outcome subgroups in the sepsis group were compared. The subgroup with SFOA score ≥ 2 points had remarkably higher levels of CK-MB and (or) cTnI than the subgroup with <2 points. The survival subgroup of CK-MB and cTnI level was remarkably higher compared to the death subgroup, the CK-MB and cTnI levels in each subgroup at 224-72 hours were remarkably higher compared to the ICU, and the difference was statistically significant (P < 0.05). Kaplan-Meier method and log-rank test indicated that the survival rates of groups 1 to 4 at 30 days were 33.23%, 78.71%, 40.03%, and 100.00%, respectively. The average survival time and their 95% CI were 12.82 d (10.52~ 16.26 d), 22.34 d (18.76~ 25.81 d), 14.65 d (11.62~ 16.38 d), and 30 d (30.00~ 30.00 d), respectively. Pairwise comparison indicated that the survival time of children in group 1 was the shortest, and that in group 4 was the longest. The results of ROC curve research showed that the CK-MB, cTnI, and SOFA scores and AUC for the combination test were 0.778 (95% CI 0.642–0.914), 0.736 (95% CI 0.602–0.890), 0.848 (95% CI 0.733–0.963), and 0.934 (95% CI 0.854–0.999), respectively. The AUC of combined diagnosis was remarkably higher compared to single factor prediction, and the difference was statistically significant (P < 0.05). Predictive value showed the joint test > SOFA score > CK − MB > cTnI. Conclusion Troponin level and pediatric SOFA score can be adopted as effective indicators to assess the severity and prognosis of patients with sepsis and can guide the formulation of a reasonable treatment plan.